ANXA7 (Annexin A7)

Protein-protein network interaction analysis showed that HSP, CD8A, C3, CD63, CD81, MRPL58, MRPL15, HNRNPA1, AMBP, IGHEP1, SERPINC1, CYP3A4, ATP12A, RPS13, CaM, HSP70 binding protein, HSPA6, C4A, ANXA7, ARG1, ARG2, ATP1B, CALCA, HTR1B, and GNGT1 are the critical proteins of leeches resistance to heat stress. Our results systematically provide substantial responsive candidate proteins combating heat stress and enhance our understanding of the intrinsic response mechanisms of thermal sensitivities animal W. pigra facing heat exposure.

This study provides new insights into overcoming resistance to BRAF and MAPK inhibitors, with implications for treating thyroid cancer and potentially other BRAF-mutant tumors. Future efforts will focus on high-throughput screening approaches to explore ANXA7-targeted therapeutic strategies for thyroid cancer.

The differentially expressed proteins provide insights into the molecular mechanisms underlying the progression of oral premalignant lesions to malignant phenotypes. The study has translational value for early detection, risk stratification, and potential therapeutic targeting of oral premalignant lesions and in its prevention to malignant forms.

Additionally, UHRF1 knockdown significantly inhibits xenograft tumor growth in vivo. In conclusion, UHRF1 knockdown inhibits proliferation and invasion, induces cell cycle arrest and apoptosis in breast cancer cells via the ZBTB16/ANXA7/Cyclin B1 axis, and reduces xenograft tumor growth in vivo.

Interestingly, among DEPs, 11 related genes (ACTB/ANXA7/C3/IGSF8/LAMC1/LGALS3/PCD6IP/SFN/TPM3/VARS/YWHAZ) for mPDAC-EVs and 9 (ACTB/ALDH2/GAPDH/HNRNPA2B/ITGA2/NEXN/PKM/RPN1/S100A6) for KPC-EVs were significantly overexpressed in tumor tissues according to gene expression profiling interaction analysis (GEPIA). Concerning the potential clinical relevance of these data, the cluster of ACTB, ITGA2, GAPDH and PKM genes displayed an adverse effect (p < 0.05) on the overall survival of PDAC patients.

SODD expression was decreased with the down-regulation of ANXA7. Down-regulating ANXA7 in Hca-P cells decreased proliferation, migration and invasion of tumor cells.

We demonstrate that fibrillization of A7-PRD proceeds via primary nucleation and fibril-catalyzed secondary nucleation processes, as determined by chemical kinetics, providing a mechanistic basis for its amyloid assembly. This study confirms and highlights a subclass of eukaryotic PRDs prone to forming aggregates with important physiological and pathological implications.

Circ-ANXA7 enhances DDP resistance in NSCLC via absorbing miR-545-3p to target CCND1 and might be a latent therapeutic target for NSCLC.